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Clin Med - Cardio Exam #1 > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

What organ produces most of the body’s cholesterol (where does the rest come from)

A

The Liver (75-80%), the rest from the diet

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2
Q

Stats about Hyperlipidemia?

A

1:6 Americans have high cholesterol
1:3 of those are treated and in good control
Less than have of those diagnosed with high cholesterol are receiving treatment

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3
Q

What is dyslipidemia?

A

The elevation of plasma cholesterol, triglycerides or both or an elevation of a low density lipoprotein level (LDL)

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4
Q

3 Types of triglycerides

A

1) Saturated - Has greatest impact on increasing LDL (all carbons fully saturated with hydrogens). (from Meat, dairy, and exotic oils
2) Monosaturated - OK in moderation from vegetable oils, peanuts and avocados.
3) Polyunsaturated - Best for you, only essential fats.. from Sunflower, safflower oils and cold water fish

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5
Q

_______ carries 60-70% of total serum cholesterol

A

LDL

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6
Q

Mono and Polyunsaturated triglycerides are only good for you in what conditions

A

Liquid form and at room temperature

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7
Q

The higher the density of cholesterol ______

A

The lower the lipid content

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8
Q

What is a lipoprotein comprised of?

A

A lipid and an apoprotein

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9
Q

What is the rate limiting step in the cholesterol synthesis process

A

The enzyme HMG CoA reductase

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10
Q

Classifications of Hyperlipidemia/Dyslipidemia

A

Primary and Secondary

Increase in cholesterol, Triglycerides or both

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11
Q

What is Primary Hyperlipidemia?

A

A single or multiple genetic mutation that results in the overproduction or defective clearance of cholesterol usually due to a defect in an apoprotein.

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12
Q

What are the 3 types of Primary Hyperlipidemia

A

1) Familial hypercholesterolemia - An increase in LDL
2) Familial combined hyperlipidemia - An increase in both LDL and VLDL
3) Familial hypertriglyceridemia - An increase in triglycerides (usually autosomal dominant)

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13
Q

What is the big dangers of familial hypertriglyceridemia?

A

50% of these patients have an MI under age 60

More at risk for pancreatitis

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14
Q

What to do if diagnosed with primary hyperlipidemia

A

Test all family members

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15
Q

What are the lab findings of Type IIa Hypercholesteromia?

A

TG normal, Increase LDL and cholesterol

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16
Q

What is the defect found in Type IIa Hypercholesteromia?

A

An LDL recepotor defect

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17
Q

What are the clinical features of Type IIa Hypercholesteromia?

A

Premature vascular disease, xanthomas. Onset found at all ages. Untreated life expectancy = 20 years

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18
Q

What is the therapy of Type IIa Hypercholesteromia?

A

Low fat/low cholesterol diet, MEDS, intestinal bypass

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19
Q

What is secondary hyperlipidemia?

A

High cholesterol due to a significant secondary cause because patients tend to have an athrogenic combination of high TG, high LDL fractions or low HDL

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20
Q

Environmental/medical risk factors for secondary hyperlipidemia?

A 
Sedentary lifestyle
Excessive intact of bad fats and cholesterol
DM or Metabolic syndrome
ETOH or tobacco use
Chronic Kidney disease/nephrosis
Hypothyroidism
Cholestatic liver disease
Medications
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21
Q

What medications can contribute to secondary hyperlipidemia?

A 
Thiazides/beta blockers
Cyclosporine
Retinoids
Estrogens and progesterone
Anabolic and corticosteroids
Carbamazepine
Protease inhibitors
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22
Q

Risk factors of secondary hyperlipidemia for people with Type 2 DM. (how does it happen?)

A

Combo of obesity, poor control or both resulting in an increase FFA.
An increase in FFA leads to an increase liver VLDL production. TG rich VLDL then transfers TG and cholesterol to LDL and HDL. That promotes formation of TG rich, small dense LDL and clearance of TG rich HDL

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23
Q

What is the pathology of hyperlipidemia?

A

Deposits of cholesterol in vascular walls creates Fatty streaks that become fibrous plaques. This creates less elasticity of the walls and a narrowing of the vessels (stenosis). Inflammation causes plaque instability leading to plaque rupture that can lead to MI, TIA and CVA

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24
Q

Factors to consider with hyperlipidemia when taking a patient’s history?

A

CV disease, Liver problems, thyroid problems, a review of medications, family history.

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25
Q

Factors to consider with hyperlipidemia when taking the patient’s physical exam?

A

Patient’s BMA, Xanthelasma’s on eyelids, Xanthomas (AT, patella, back of hand, buttocks), cream color in blood, signs of ETOH abuse, DM or Metabolic syndrome

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26
Q

Current labs for hyperlipidemia workup

A

Fasting glucose, LFT’s, Chem panel, TSH and Urine protein

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27
Q

What is the definition of Metabolic Syndrome?

A

A cluster of common conditions that increase T2DM and CVD risk.

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28
Q

What is the criteria for metabolic syndrome

A

Must have 3 of the following
- Abdominal obesity
(waist circumference >40” men, >35” women)
- Impaired glucose tolerance
(Fasting plasma glucose >100 mg/dL or on a specific
med or diagnosed with T2DM
- Low HDL
(Males 150 mg/dL or on a specific med)
- HTN
(BP >130 mmHg systolic, 85 mmHg diastolic or on
specific med)

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29
Q

What is the Framingham test?

A

Test to determine CVD risk in Asymptomatic patients within 10 years

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30
Q

What are the Framingham test scores

A

Score under 10% is low risk
Score btwn 10-20% is intermediate risk
Score 20% = High risk

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31
Q

Metabolic syndrome aliases

A 
Dysmetabolic syndrome
Hypertriglyceridemic waist
Insulin resistance syndrome
Obesity syndrome
Syndrome X
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32
Q

What are the different guidelines of cholesterol testing

A

National Cholesterol Education Program (NCEP)
adults 20 or over every 5 years
US Preventative Task Force (USPSTF)
Total cholesterol and HDL every 5 years
All men over 35
Women 45 and over if @ increase for CHD
Men 20-35 and women 20-45 if increase CHD risk

33
Q

What are the equations to determine lipids in the lab

A

1) Total cholesterol = HDL + LDL + VLDL
2) VLDL = TG/5
3) LDL = Total cholesterol - HDL - TG/5

34
Q

What are the guidelines for total serum cholesterol

A

Under 200 -desirable
200-239 - Borderline High
240 and over - High
(Over 150 is associated with CHD risk)

35
Q

What are the guidelines for serum LDL

A 
Under 100 - optimal
100-129 - Near/above optimal
130-159 - Borderline High
160-189 - High
Over 190 - Very high
36
Q

What is the LDL goal for drug therapy

A

Try to achieve a 30-40% reduction (60% is ideal)

37
Q

What are the goals for Serum HDL

A

Under 40 - Low

Over60 - High

38
Q

What the NCEP ATP III recommendations for Framingham scores and Hyperlipidemia

A

Low Risk - LDL goal/initiate chng 160, drug therapy >190
Mod Risk - LDL goal/change 130, drug therapy > 160
Mod/High - LDL goal/change 130, drug therapy > 130
High Risk - LDL goal/change 100, drug therapy >100

39
Q

For every ______ decrease in serum cholesterol, CV risk decreases by _____

A

1% decreases by 2%

40
Q

Saturated fat vs. Dietary cholesterol on Serum Cholesterol

A

Sat. fat has much more of an influence than dietary cholesterol.
Changes in dietary cholesterol gives a modest benefit, reducing dietary saturated fats can decrease serum cholesterol by 10%

41
Q

What are some dietary considerations with hyperlipidemia

A

1) Consume less than 10% of calories from saturated fat
2) Consume less than 300 mg/day of cholesterol
3) Keep trans fatty acid consumption low as possible
4) Emphasize fruits, vegetables and whole grains

42
Q

What are some things that can raise HDL levels (and by how much)

A

Exercise 30 min/day - 5-20%
Weight loss - 5-10%
Modest ETOH use - 1-2 oz daily
A handful of unsalted walnuts, almonds or pecans at bedtime

43
Q

Under the new guidelines what is the Framingham score that you would start treating someone for Hyperlipidemia

A

7.5% CVD risk in 10 years

44
Q

What are the treatment goals of Hyperlipidemia/dyslipidemia?

A

LDL goal for low risk and no co-morbidities 20% Framingham score)

45
Q

What are the 4 classes of Cholesterol meds (and 2 others)?

A

1) HMG CoA reductase inhibitors (STATINS)
2) Bile Acid Sequestrants
3) Fibric Acids
4) Nicotinic Acids
ALSO - Zetia (for those with Statin sensitivities and Omega 3)

46
Q

What are the 1st and 2nd choices of drug therapy for Hyperlipidemia? (how much will it improve)

A

1st choice - Statins (HMG-CoA reductase inhibitors)
Can lower CVD risk - 20-30%
Lower LDL count - 14-63%
2nd choice - Ezetimibe (Zetia) - those with Statin intolerance
Lower LDL count - 15-20%

47
Q

What do all HMG CoA reductase Inhibitor drugs end in?

A

-statin

48
Q

What are the 6 Statin drugs?

A

Atorvastatin, fluvastatin, lovastatin, pravastatin, rosuvastatin and simvastatin

49
Q

With is the MOA for HMG COA reductase Inhibitor (statins)?

A

They inhibit rate limiting enzymes in the formation of cholesterol. Give a small increase in HDL and a moderate decrease in LDL

50
Q

What are the side effects of HMG COA reductase Inhibitor (statins)?

A

Myositis, and there are questions about them causing diabetes

51
Q

What are some adverse effects of HMG COA reductase Inhibitor (statins) and what needs to be done about it?

A

Liver toxicity - Need to obtain LFT baseline when initiating
- Don’t need to monitor but d/c if ALT/AST is 3x
baseline
Rhabdomyolysis with acute renal failrure
- Need a baseline CPK
- Counsel patient to report any muscle pain,
tenderness. weakness or brown urine

52
Q

What is the MOA of Exetimibe (Zetia)?

A

It blocks intestinal absorption of dietary and biliary cholesterol

53
Q

What are three Bile acid-binding resins?

A

1) Cholestyramine
2) Colestipol
3) Colesevelam

54
Q

What is the MOA of Bile acid-binding resins?

A

Binds bile acids in the gut and reduces enterohepatic circulation of bile acids, resulting in increased liver production of bile acids using hepatic cholesterol

55
Q

What are the effects of Bile acid-binding resins?

A

Decreases LDL by 15-25%
No effect on HDL
20% reduction in CHD events

56
Q

What is the only lipid lowering agent that is considered safe in pregnancy

A

Bile acid-binding resins

57
Q

What are three Fibric acid derivative drugs

A

1) Gemfibrozil
2) Fenofibrate
3) Clofibrate

58
Q

Who is Fibric acid derivative drugs most useful for and what are their MOA.

A

Most useful in those with high TG and low HDL

They reduce synthesis and increase breakdowns of VLDL.

59
Q

How effective are Fibric acid derivative drugs?

A

Can reduce LDL by 10-15% and reduce TG by 40% and increase HDL by 15-20%

60
Q

What is a major warning of clofibrate?

A

Has had an increased level of cancer in a large clinical trial

61
Q

What are the sfx of Fibric acid derivative drugs?

A

Gallstones (cholelithiasis), hepatitis and myositis

62
Q

What does Niacin do to treat Hyperlipidemia?

A

Reduces production of VLDL and decreases LDL by 15-25%.
It raises HDL by 25-35%
Decreases TG by 50%
Lowers Lp(a) and homocysteine levels

63
Q

What are the sfx of Niacin?

A

Flushing. You can take an ASA prior to dosing to help prevent this

64
Q

What does Omega 3 Oils do for Hyperlipidemia?

A

Lower triglycerides, they don’t lower mortality or risk of CV disease or events

65
Q

Warnings for Omega 3 Oils

A

Pregnancy category C
D/C if no response after 2 months
Watch for those with fish/shellfish allergy/sensitivity
Freeze capsules if it causes GERD

66
Q

Name 5 combination drug therapies for Hyperlipidemia

A

Statin + bile acid sequestrant
Statin + fibric acid derivative (not gemfibrozil)
Statin + niacin
Statin + fibric acid derivative (not gemfibrozil) + niacin
Statin + cholesterol absorption inhibitor

67
Q

Start treating any patient (any age or healthy) when their LDL’s go above _____

A

190 mg/dL (start treating with a statin)

68
Q

Start treating a patient with risk factors (like DM) when LDLs are ______

A

70 - 189 mg/dL (moderate dose of a statin). A high dose of they have above a 7.5% risk factor on Framingham scale

69
Q

T/F Unexplained myalgias may occur on statins w/o CK elevation.

A

False, minimal but nothing requiring you to stop

70
Q

Statins have drug interactions with _______

A

CYP3A4 inhibitors

71
Q

What are examples of CYP3A4 inhibitors?

A

Macrolides, azole antifungals, cyclosporins, telithromycin, danazol, amiodaroine, verapamil

72
Q

What is the exception of a statin that doesn’t have drug interactions with CYP3A4 inhibitors? (why?)

A

Pravastatin (It’s metabolized in the gut rather than the liver)

73
Q

What is the Fibrate that especially interacts with statins (why?)

A

Gemfibrozil (inhibits metabolism, raises statin in blood and can create a toxicity)

74
Q

Niacin and statins can cause ______

A

Myalgias

75
Q

What are better medicines that should be used to lower LDL - C

A

1) Bile acid sequestratnts
2) Nicotinic Acid
3) Fibrates

76
Q

What are better medicines that should be used to lower triglycerides?

A

1) Fibrates
2) Nicotinic acid
3) Omega 3 Fatty acids

77
Q

What are better medicines that should be used to enhance HDL - C

A

1) Stains, Fibrates and Bile acids

2) Nicotinic acid

78
Q

What drugs have zero affects on enhancing HDL

A

Ezetimibe and Omega 3’s

Clin Med - Cardio Exam #1 (7 decks)

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